Kim Young Min, Ha Yu Mi, Jin Yong Chun, Shi Lian Yu, Lee Yong Soo, Kim Hye Jung, Seo Han Geuk, Choi Jae Soo, Kim Yeong Shik, Kang Sam Sik, Lee Jae Heun, Chang Ki Churl
Department of Pharmacology, School of Medicine, and Institute of Health Sciences, Gyeongsang National University, 92 Chilamdong, Jinju, Republic of Korea.
Food Chem Toxicol. 2009 Aug;47(8):2097-102. doi: 10.1016/j.fct.2009.05.031. Epub 2009 Jun 2.
The aim of the present study was to evaluate the protective effect of palmatine, one of active ingredients of Coptidis rhizoma, against myocardial ischemia-reperfusion (I/R) injury is due to its antioxidant and anti-inflammatory action. Adult male rats were subjected to 30 min of ischemia and 6 or 24h of reperfusion. Rats were randomized to receive vehicle or palmatine 1h before reperfusion. Infarct size, myocardial function, and the antioxidant enzyme activity, such as malonaldehyde (MDA), lactate dehydrogenase (LDH), creatine phosphokinase (CK), superoxide dismutase (SOD) and catalase (CAT) were measured. Palmatine significantly improved I/R-induced myocardial dysfunction by increasing the values of the first derivative (+/-dp/dt) of left ventricular pressure and decreased infarct size by 50% (P<0.01 versus vehicle). As expected, palmatine markedly inhibited the increase of LDH, CK, and MDA contents in I/R rat serum, and it also significantly inhibited the decline of the activity of SOD and CAT in I/R cardiac tissues. In addition, COX-2 and iNOS expression in I/R myocardium was significantly reduced. Interestingly, palmatine increased heme oxygenase (HO)-1 induction in human aortic endothelial cells. We concluded that palmatine protects hearts from I/R injury in rats possibly by reducing oxidative stress and modulating inflammatory mediators.
本研究的目的是评估黄连根茎的活性成分之一巴马汀对心肌缺血再灌注(I/R)损伤的保护作用,其作用机制可能是通过抗氧化和抗炎作用。成年雄性大鼠经历30分钟的缺血和6或24小时的再灌注。大鼠在再灌注前1小时随机接受溶剂或巴马汀处理。测量梗死面积、心肌功能以及抗氧化酶活性,如丙二醛(MDA)、乳酸脱氢酶(LDH)、肌酸磷酸激酶(CK)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)。巴马汀通过增加左心室压力的一阶导数(+/-dp/dt)值显著改善I/R诱导的心肌功能障碍,并使梗死面积减少50%(与溶剂组相比,P<0.01)。正如预期的那样,巴马汀显著抑制I/R大鼠血清中LDH、CK和MDA含量的增加,并且还显著抑制I/R心脏组织中SOD和CAT活性的下降。此外,I/R心肌中COX-2和iNOS的表达显著降低。有趣的是,巴马汀增加了人主动脉内皮细胞中血红素加氧酶(HO)-1的诱导。我们得出结论,巴马汀可能通过降低氧化应激和调节炎症介质来保护大鼠心脏免受I/R损伤。